The syndromes of bulimia nervosa and anorexia nervosa are serious psychiatric disorders characterized by abnormal eating patterns with psychological symptoms involving preoccupation with body shape and weight. These disorders are estimated to affect two to five per cent of women (and a smaller number of men) of high school and college age, the population at highest risk. Neurobiological alterations may contribute to the initial onset and/or to the perpetuation of symptoms in these disorders. There is much current interest in the hypothesis that impaired central serotonin function contributes to blunted post-prandial satiety responses in patients with bulimic symptoms (i.e., bulimia nervosa patients at normal weight, or low weight anorexic patients with the additional features of bulimia nervosa). This hypothesis is consistent with preclinical studies demonstrating a major role for hypothalamic serotonin in mediating meal-induced satiety. Preliminary evidence for reduced serotonin function in normal weight bulimic patients has emerged from studies of pharmacological/neuroendocrine challenge responses, cerebrospinal fluid metabolites, and pharmacological treatment studies. There is suggestive evidence for decreased serotonin function in bulimic anorexic patients in comparison to nonbulimic anorexic patients. Utilizing single-blind, placebo-controlled acute pharmacological.challenge with the serotonin agonist fenfluramine, this study will compare neuroendocrine responses in currently symptomatic female bulimic patients at normal weight, in symptom remitted bulimic patients, and in age- and sex-matched controls. Clinical variables such as duration and severity of bulimic symptoms, body weight and dietary pattern, severity of depressive symptoms, and alterations in menstrual function will be evaluated as possible predictors of altered serotonergic responsiveness. This study will provide new data on the possible role of central serotonergic alterations in the pathophysiology of bulimia nervosa.